Journal of Medical Virology · 2016 · 44 citations · 48 references
Veterinary MedicineImmunologyInfectious DiseasesImmunogeneticsInflammationInnate ImmunityCytokine BiologyCytokine DysregulationCytokine Gene PolymorphismHepatocellular CarcinomaLiver DiseaseViral HepatitisHepatitis C InfectionHepatocellular Carcinoma PathogenesisInflammation In Liver InjuryInflammatory Response GenesInterleukin-10 Gene VariantsTh1 Th2 BalanceTumor Necrosis Factor Alpha VariantsTumor Necrosis Factor Gene Variants
Hepatitis C virus (HCV) is the major cause of hepatocellular carcinoma (HCC). The risk to develop HCC increases with the severity of liver inflammation and hepatic fibrosis. It is believed that a balance between the releases of pro- and anti-inflammatory cytokines will determine the clinical course of HCV and the risk to develop HCC. The inteleukin-10 (IL-10) and the tumor necrosis factor alpha (TNF-α) play key roles in the Th1 and Th2 balance during the inflammatory response against HCV. The aim of the present study was to investigate the association between polymorphisms in TNF-α -308 G>A (rs1800629), IL-10 -1082 G>A (rs1800896) and -819/-592 (rs1800871/rs1800872) with HCC risk in individuals with HCV. The present study evaluated 388 chronic HCV patients. Polymorphisms were determined by real-time PCR. Diplotypes associated with low IL-10 production and the TNF-α GG genotype were significantly associated with HCC occurrence after multivariate logistic regression analysis (P = 0.027 and P = 0.029, respectively). Additionally, the IL-10 -819 (-592) TT (AA) genotype was significantly associated with multiple nodules and HCC severity according to BCLC staging (P = 0.044 and P = 0.025, respectively). Patients carrying low production haplotypes of IL-10 and the TNF-α GG genotype have higher risk to develop HCC. J. Med. Virol. 88:1587-1595, 2016. © 2016 Wiley Periodicals, Inc.
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